holoacardius : a separate, monozygotic
twin represented by a more or less shapeless and unidentifiable mass; the
vascular systems of the 2 fetuses are connected, and the circulation is
accomplished solely by the heart of the more perfect twin.

acardius or holoacardius acephalus : an imperfectly formed free
twin fetus lacking the cranial part of the body

acardius or holoacardius acormus : an imperfectly formed free twin
fetus lacking the caudal part of the body

acardius or holoacardius amorphus : an imperfectly formed free twin
fetus entirely without form and recognizable parts

acardius anceps / hemiacardius :
one of twin fetuses in which only a part of the circulation is accomplished
by its own heart.

celosomian monster / celosomus / kelosomus
: a fetus exhibiting celosomia, a developmental anomaly characterized
by fissure or absence of the sternum and hernial protrusion of the viscera

strophosomus : a celosomus, especially in chicks, in which the extremities
are reflexed onto the back with the distal ends resting on the head.

toxoplasmosis,
other agents, rubella,
cytomegalovirus,
herpes
simplex
(TORCH) infection or syndrome : any of a group of infections seen in
neonates due to one of the causative agents having crossed the placental
barrier; they all have similar symptoms in babies and may be clinically
silent in the mothers

dicephalus dipus dibrachius : a fetus with 2 heads but only 2 feet
and 2 arms.

dicephalus dipus tetrabrachius : conjoined twins with only 2 legs,
but with varying degrees of fusion of the upper trunk, each component having
a head and pair of arms.

dicephalus dipus tribrachius : a fetus with 2 heads, 2 feet, but
with a median third arm or arm rudiment.

dicephalus dipygus / anakatadidymus : conjoined twins that are separate
above and below, but united in the middle

dicephalus parasiticus / desmiognathus : a fetus with a parasitic
head attached to the jaw or neck

dicephalus tripus tribrachius : a fetus with a common trunk, but
with 2 heads, 3 arms, and 3 legs, the third limbs being either rudimentary
or complete.

anadidymus / duplicitas inferior or posterior : conjoined twins
that are divided below but single toward the cephalic pole

those in which only a small
part of the body is duplicated or one small and incompletely developed
parasitic twin is attached to a much larger and more fully developed twin
(incomplete, unequal or asymmetrical conjoined twins / heteropagus /
compound, double or twin monster)

autosite / autositic monster : the larger,
more nearly normal component of asymmetrical conjoined twins, to which
the parasite is attached as a dependent growth

parasite / parasitic monster : the smaller,
less complete component of asymmetrical conjoined twins, which is attached
to and dependent on the autosite.

teratoid parasite : in asymmetrical conjoined twins, a parasite
that appears as a tumorlike mass.

polysomus : conjoined twins exhibiting polysomia.

parasitic monster : in asymmetrical conjoined twins, the smaller,
imperfect twin, which is unable to exist alone and is attached to or derives
its nutrition from the circulation of the larger, more perfectly developed
twin

heterodymus : asymmetrical conjoined twins
in which one fetus has a second head, neck, and thorax attached to its
thorax.

monocephalus / monocranius : a fetus with one head but with some
duplication of its parts.

monocephalus tetrapus dibrachius : conjoined twins with one head,
two arms, and partial or complete duplication of the pelvis, with 4 legs,
the pair belonging to one member often being fused in a single limb.

monocephalus tripus dibrachius : conjoined twins with one head,
2 arms, and partial duplication of the pelvis, with a median third leg
or leg rudiment.

encranius : in asymmetrical conjoined twins, a parasitic twin located
within the cranium of the larger twin.

craniopagus / cephalopagus : conjoined
twins united by the heads

Epidemiology : incidence = 1 in 2.5 million
births.

craniopagus occipitalis : craniopagus in which fusion is in the
occipital regionref1,
ref2

craniopagus parietalis : craniopagus in which fusion is in the parietal
regionref.
Ladan
and Laleh Bijani were craniopagus sisters born on January 17, 1974
in Shiraz, a city in southwest Iran, to Dadollah Bijani and Maryam Safari,
members of a farming family from Lohrasb.

The Bijani sisters were lost in the hospital in 1979 after the doctors
responsible for them fled back to the United States during the Islamic
revolution. The Bijanis' parents did not find the sisters again until several
years later in Karaj, where Dr. Alireza Safaian found and adopted them.
Even though Dadollah Bijani won the custody against Safaian, the sisters
chose to spend their childhood with Safaian. Since they had to study together,
they needed to choose a common career path. Ladan wanted to be a lawyer,
while Laleh wished to become a journalist; in the end, they settled on
Ladan's choice and studied law for 4 years at Tehran University. Most other
personal decisions also had to meet each other's approval. For these and
other reasons, they had wanted to be separated since they were youngsters.
Laleh hoped that she could then move to Tehran, the capital city of Iran,
to study journalism, while her sister continued with a graduate studies
in law and then move to Shiraz. In addition, the sisters had different
hobbies. While Laleh liked to, among other things, play computer games,
Ladan preferred computer programming. Ladan also described her sister as
more introverted and herself quite talkative. Although they lived all their
lives together they never saw each other’s faces directly. Laleh’s biggest
wish was to see her sister’s face without the mirror. In 1996, they travelled
to Germany, trying to get doctors there to separate them; the German doctors
however declined to operate, saying that the risk of separation surgery
would be too high for both of them. In November 2002, after meeting Dr.
Keith Goh, a Singaporean neurosurgeon who successfully separated the Shrestha
sisters (Ganga and Jamuna), who had previously also been joined
at the head, the Bijani sisters travelled to Singapore to undergo the controversial
operation. Their decision to go ahead with the operation though they were
warned by the doctors that they had a 50-50 chance of survival caused a
media blitz internationally. Just before the operation took off they jointly
wrote a letter to their numerous friends and well-wishers thanking them
for their support and encouragement. After 7 months in the Southeast Asian
country doing extensive psychiatric and legal evaluations, they went to
the operating table on July 6, 2003, under the care of a large team of
international specialists at Raffles
Hospital, composed of 24 surgeons and > 100 support staff working in
shifts. Professor Lewis Spitz, who has managed 23 sets of conjoined twins
at the Great Osmond Street Hospital in London, was a member of a South
African team that successfully separated twins joined at the skull and
sharing a major blood vessel in 1968 (though much less complicated, 1 of
the twins died 6 months after). The attempt to separate the twins turned
out to be very difficult, because their brains not only shared the superior
sagittal sinus, but had fused together.
At around 10:00, surgery began and the femoral vein was harvested after
the saphenous vein was found to be too small. The separation was achieved
on July 8, 2003 after 50 hours of general anaesthesia, but it was announced
then that the twins were in critical condition.
The angiogram that was supposed to reveal the Bijanis' vascular structure
did not pick up a vein that spanned the base of the twins' skulls. Only
after nearly 30 hours of surgery did doctors discover the vein, which had
become a major drainage pathway. When surgeons severed the vein, they were
unable to stop the bleeding. The separation stage of the surgery completed
at 13:30 (Singapore time, UTC +8), but there was significant blood loss
during the blood vessel repairing process, and Ladan Bijani died at around
14:30 on the operating table; her sister Laleh died a short time afterwards
at 16:00ref1,
ref2.
The deaths were announced by the chairman of Raffles Hospital, Dr. Loo
Choon Yong. The sisters were buried in accordance to Shiite Muslim traditions
in separate tombs, side by side, in Lohrasb. The sisters willed their property
to blind and orphaned children. How not to remember the end phrase of the
"Hey you" song by Pink Floyd : "Together we stand, divided we fall."

craniopagus parieto-occipitalis

metopopagus : a craniopagus in which the
fusion is in the region of the forehead.

craniopagus parasiticus / epicome
:
craniopagus in which a parasitic head is attached to the head of the larger,
more nearly normal twin. It results from compromise of the blood supply
to one of a pair of craniopagus conjoined twins. It differs from craniopagus
conjoined twins in that the body and limbs of the parasitic twin are underdeveloped,
leaving in some cases only a parasitic head, inserted on the crown of the
autositic twin. The infant is otherwise healthy but her brain cannot develop
normally unless the undeveloped head is removed. There have only been 8
documented cases in the worldref1,
ref2,
ref3,
ref4,
and 1 only case where surgery has been attempted to correct itref5.
The first case of this malformation was Everard Home's famous Twin-Headed
Boy of Bengal, whose skull is preserved at the Hunterian Museum. A ninth
case occurred in Dominican Republic : Rebeca
Martinez was born in Dec 10 2003 from 26-year-old mother Maria Gisela
Hiciano and 29-years old father Franklyn Martinez (which have 2 other children
ages 4 and 1) at a hospital in Santo Domingo. On Feb 6, 2004, the medical
team led by neurosurgeons Dr. Jorge Lazareff (director of pediatric neurosurgery
at the University of California at Los Angeles' Mattel Children's Hospital)
and Dr. Benjamin Rivera (at the CURE International Center for Orthopedic
Specialties) completed the operation on the 8-week-old girl, which doctors
believe to be the first of its kind, in nearly 14 hours, saying it went
smoothly : 18 surgeons, nurses and doctors took several rotations to cut
off the undeveloped tissue, clip the veins and arteries, and close the
skull using a bone and skin graft from the second head. The operation was
critical because the head on top was growing faster than the lower one
and without an operation the child would barely be able to lift her head
at 3 months old. After what seemed to be a very successful surgery that
ended about 10:30 last evening, post-op hemorrhaging caused doctors to
perform surgery again at 1:30am to try and stop the bleeding : she passed
away early the morning of Feb 7 around 8am

The 10-month-old Egyptian baby Manar Maged had an operation
to remove a parasitic head in Feb 2005 and a second operation to treat
hydrocephalus at Benha Children's Hospital north of Cairo.

gastroacephalus : asymmetrical conjoined twins in which the larger
twin bears the smaller one as a headless parasite on its abdomen.

dipygus : a fetus with a double pelvis

gastrothoracopagus : conjoined twins joined at the abdomen and thorax.

gastrothoracopagus dipygus / dipygus parasiticus : asymmetrical
conjoined twins in which there is attached to the abdomen of the larger
twin a parasitic twin consisting of the pelvis and lower limbs only

engastrius : asymmetrical conjoined twins with the parasitic twin
contained within the abdomen of the larger twin.

miodidymus : asymmetrical conjoined twins in which a smaller head
is joined to the larger one at the occiput.

cryptodidymus / endadelphos : asymmetrical conjoined twins in which
a parasitic fetus is enclosed within the body of or within a tumor upon
the larger twin. It is different from fetus in fetu (a well-differentiated
fetal teratoma having axial formation of limbs and organs)

thoracopagus / thoracodidymus : conjoined twins united in or near
the sternal region, so the two components are face to face

thoracopagus epigastricus : asymmetrical conjoined twins in which
the parasitic twin is attached to the epigastric region of the larger twin.

thoracopagus parasiticus : asymmetrical conjoined twins in which
the parasitic twin is attached to the thorax of the larger twin.

thoracoparacephalus : asymmetrical conjoined twins, a parasitic
twin with rudimentary head being attached to the thorax of the larger twin

cephalothoracopagus : conjoined twins united at the head, neck,
and thorax.

cephalothoracopagus disymmetros : a cephalothoracopagus fused squarely
in the frontal plane and presenting 2 broad anterior surfaces and two narrow
posterior ones, with a common head bearing 2 faces, each being formed by
the right and left halves of the different components.

cephalothoracopagus monosymmetros : a cephalothoracopagus with 1
complete face formed by a right and a left half of the 2 components, the
other face being only rudimentary.

pygoamorphus : asymmetrical conjoined twins in which the parasite
is an amorphous mass attached to the sacral region of the more developed
twin

caudal regression syndrome
/ caudal dysplasia syndrome / caudal regression syndrome / sacral agenesis
: failure of formation of part or all of the coccygeal, sacral, and occasionally
lumbar vertebral units and the corresponding segments of the caudal spinal
cord, with resulting neurogenic dysfunction of bowel and bladder. A rare
syndrome which has a spectrum of congenital malformations ranging from
simple anal atresia to absence of sacral, lumbar and possibly lower thoracic
vertebrae, to the most severe form which is known as sirenomelia
with lower extremity fusion and major vessel anomalies.

segmental spinal dysgenesis
(SSD) is a rare congenital abnormality in which a segment of the spine
and spinal cord fails to develop properly. SSD and caudal regression syndrome
probably represent two faces of a single spectrum of segmental malformations
of the spine and spinal cord. The neuroradiologic picture depends on the
severity of the malformation and on its segmental level along the longitudinal
embryonic axis. The severity of the morphologic derangement correlates
with residual spinal cord function and with severity of the clinical deficit

impacted twins : twins so situated during delivery that the pressure
of one against the other prevents simultaneous engagement of both

dysmaturity
or postmaturity syndrome / placental dysfunction syndrome : a syndrome
due to placental insufficiency that causes chronic stress and hypoxia,
seen in fetuses and newborn infants in post-term pregnancies and characterized
by decreased subcutaneous fat, skin desquamation, and long fingernails,
often with yellow meconium staining of the nails, skin, and vernix

fetal
alcohol syndrome (FAS) : suppression of nerve cell activity, required
to form connections and thrive in a baby's growing brain, leads to neuronal
apoptosis. FAS is a syndrome of altered prenatal growth and morphogenesis
occurring in infants born of women who were chronically alcoholic (ethanol
addicted) during pregnancy; it includes maxillary hypoplasia, prominence
of the forehead and mandible, short palpebral fissures, microphthalmia,
epicanthal folds, severe growth retardation, mental retardation, and microcephaly.

fetal hydantoin syndrome :
a symptom complex characterized by poor growth and development with craniofacial
and skeletal abnormalities, produced by prenatal exposure to hydantoin
analogues, including phenytoin

CHARGE association : a syndrome
of associated defects, including coloboma of the eye, heart
anomaly, choanal atresia, retardation, and genital
and ear anomalies. Facial palsy, cleft palate, and dysphagia are
often present, and familial transmission has been postulated

malnutrition / hypothrepsia : any disorder
of nutrition; it may be due to unbalanced or insufficient diet or to defective
assimilation or utilization of foods.

deficiency or deprivation
disease : a condition produced by dietary or metabolic deficiency;
the term includes all diseases caused by an insufficient supply of the
essential nutrients, i.e., protein (or amino acids), vitamins, and minerals.

beriberi

scurvy

pellagra

calcium deficiency

fat-deficiency disease : a
condition characterized by cessation of growth and skin lesions that result
when essential fatty acids (linolenic and linoleic acid) are absent from
the diet.

protein-energy malnutrition
(PEM) : a class of disorders caused by varying degrees of protein and
calorie deficiency, alone or in combination, frequently aggravated by accompanying
physiologic and environmental stresses

primary PEM

marasmus / infantile atrophy / athrepsia / pedatrophia
: a form of PEM predominantly due to prolonged severe caloric deficit,
chiefly occurring during the first year of life, characterized by growth
retardation and progressive wasting of subcutaneous fat and muscle, but
usually with retention of the appetite and mental alertness. Infectious
diseases may be precipitating factors for starvation
acidosis or ketoacidosis

kwashiorkor / malignant malnutrition / protein
malnutrition : a form of protein-energy malnutrition produced by severe
protein
deficiency; caloric intake may be adequate but is usually also deficient.
It is characterized by retarded growth, changes in skin and hair pigment,
edema, enlarged abdomen, immunodeficiency, and pathologic changes in the
liver, including fatty infiltration, necrosis, and fibrosis. Other findings
are mental apathy, atrophy of the pancreas, gastrointestinal disorders,
anemia, low serum albumin, and dermatoses. The skin of the limbs and back
may have dark thickened patches, which may desquamate, leaving pink, almost
raw surfaces.

Symptoms & signs : flag sign
: dyspigmentation of the hair occurring as a band of light hair, seen in
children who have recovered from kwashiorkor.

marasmic kwashiorkor / nutritional
marasmus : a condition in which there is deficiency of both calories
and protein, with severe tissue wasting, loss of subcutaneous fat, and
usually dehydration.

PEM secondary to other diseases

Gopalan's syndrome / burning feet syndrome
: a symptom complex resulting from malnutrition, probably from deficiency
of riboflavin or pantothenic acid; it consists of a burning sensation in
the extremities, a feeling of “pins and needles” in the distal parts, and
hyperhidrosis

triceps skin fold (TSF) thickness measured with a skin caliper
on the posterior aspect of the nondominant arm by pinching a fold of skin
from the underlying triceps muscle. Total body fat can be estimated from
TSF with the Siri equationref.
subscapular skinfold was measured below the lower vertex of
the scapula with the skinfold caliper at 45° to vertical
abdominal skinfold was measured halfway along an imaginary line
joining the umbilicus and the anterosuperior iliac crest.
fat-muscle index

inpatients receive Formula 75 and Formula 100 (a liquid
diet with 100 kcal/100 mL. It is prepared by mixing dried skimmed milk,
oil, sugar, and a vitamin and mineral mix (without iron) with water (Golden
MHN. Severe malnutrition In: Weatherall DJ, Ledingham JGG, Warell DA, eds.
The Oxford textbook of medicine, vol 1. Oxford: Oxford University Press,
1995: 1278-1297). Specifications for its industrial preparation have been
published (UNDP-IAPSO. In: . In: Emergency relief items—compendium
of generic specifications. vol 1:Copenhagen: UNDP, 1995: 107)),
highly appropriate therapeutic milksref,
in quantities tailored to the individual's metabolic needs. Systematic
medical and supportive care complements this approach. Because F100 is
an excellent medium for bacteria, it has to be prepared before each meal
and used by experienced staff. This is a problem because recovery usually
takes 4 weeks, residential facilities are limited and expensive, and outpatient
management with F100 not advisable.

community-based therapeutic care use a new ready-to-use therapeutic
food (RUTF), specially designed to treat severe malnutrition in the
community. RUTF is a new food, designed to be nutritionally equivalent
to the Formula 100 used in therapeutic feeding centres, but is a paste
that patients can eat directly from the packet. The RTUF complied with
the F100 formula (UNDP-IAPSO. In: . In: Emergency relief items—compendium
of generic specifications. vol 1:Copenhagen: UNDP, 1995: 107),
except that part of the dried skimmed milk was replaced with lactoserum
and groundnut paste (Nutriset, France). The formula contained 543 kcal/100
g. Bacteria, when added to the product, failed to grow. The product looked
and tasted like peanut butter.Preliminary trials suggest that RUTF is popular
with malnourished children and highly resistant to contamination with bacteriaref.
RUTF is made from peanuts, dried skimmed milk, sugar, and a specially formulated
mineral and vitamin mix, and will keep for several months in a simple pot.
All the ingredients apart from the CMV are available in less-developed
countries. Instead of relying exclusively on therapeutic feeding centres,
imported foods, and large numbers of external experts, community-based
therapeutic care offers the potential to establish community structures
to address the problems of severe malnutrition with local knowledge and
locally manufactured therapeutic food. Initially, community-based therapeutic
care programmes will require considerable external facilitation with staff
and imported RUTF. However, during the course of an emergency, these requirements
will decline as the community base becomes stronger and local production
of RUTF increases. At the end of an emergency, the socalled Hearth groups
can easily reorientate themselves towards more developmental goals, while
leaving the core structures in place for reactivation should another emergency
occur. home-based or outpatient care for severe malnutrition has been attempted
in countries such as India and Bangladesh. A limiting factor has been the
difficulty of providing an appropriate nutritional product that does not
require the addition of water, since the water that is available may be
of suspect quality. Today, however, there are RUTFs that are as effective
as therapeutic milk products.

BP-100, for example, is a nutrient-fortified wheat-and-oat bar

Plumpy'nut is a peanut butter–like paste containing the balance
of lipid, sugar, and protein (macronutrients) and minerals and vitamins
(micronutrients) that promotes rapid growth in severely malnourished childrenref1,
ref2.
It comes in individual packets that are essentially immune to bacterial
contamination; and because they are sealed, single servings, they are not
likely to be shared by other children.

Neither BP-100 nor Plumpy'nut requires the addition of water, so questions
about proper dilution and the availability of clean water are eliminated.
Nor do they require cooking or other preparationref

zed reaction (a reaction which appears in infants in cases of starvation
after the starvation is relieved; it consists of a slight gain in weight,
elevation of temperature, and the appearance of watery stools containing
a large number of cells)

Pathogenesis : it causes not just the loss
of fat, but also of bone and muscle, and happens regardless of the amount
the patient manages to eat. The patient's metabolism speeds up, burning
more calories. The condition further robs patients of the ability to fight
the disease which triggered the cachexia. It is believed that cytokines
released by the body in response to the underlying illness are responsible
for the wasting illness, as TWIST
deficiency causes cachexia in experimental models

anorexia-cachexia syndrome
: a systemic response to conditions such as cancer
or the AIDS,
resulting from a poorly understood relationship between anorexia and cachexia,
manifested by malnutrition, weight loss, muscular weakness, acidosis, and
toxemia. The anorexia may be caused by a severe metabolic disturbance that
contributes to development of cachectic wasting, which in turn reinforces
anorexia by release from the tumor of a humoral product that stimulates
the satiety center in the hypothalamus

polytrauma : the occurrence of injuries to
more than one body system when energy is distributed over whole body and
overwhelming tissue resistances in some areas.

blunt thoracic injury : sufficient
trauma to the chest can result in injury to the bony thorax and soft tissues
of the chest wall, increasing patient morbidity and mortality. Fractured
ribs can lacerate the pleura, lung, or abdominal organs. Fractures to upper
ribs, clavicle, and upper sternum can signal brachial plexus or vascular
injury. Paradoxical movement of a flail chest can impair respiratory mechanics,
promote atelectasis, and impair pulmonary drainage. Most patients with
thoracic spine fracture-dislocations have complete neurologic deficits.
Scapular fractures, associated with other injuries in almost all patients,
are frequently overlooked on supine chest radiographs. Sternal fractures,
associated with clinically silent myocardial
contusion,
are best visualized on chest computed tomography (CT). Severe trauma to
the chest wall can be associated with large chest wall hematomas or collections
of air within the chest wall that can communicate with the intrathoracic
space. CT scanning can easily distinguish chest wall from parenchymal or
mediastinal injury, whereas this differentiation my not be possible with
chest radiography.

blunt abdominal trauma (BAT)
or injury

Epidemiology : leading cause of death in USA
between age 1 and 34; 150,000 deaths per year; 60 millions traumatized
patients per year; 200 billion US$ per year in health care expenses
Aetiology : traumatopathy

external hemorrhages : tamponade or pressure until arrival in operatory
room (hemostasis is not required and tourniquet closes only superficial
veins). Penetrating injuries may be closed with Foley's catheter with closed
tip and inflated balloon

log-roll : method of turning a patient without twisting the spine,
used when a person's spine is unstable; backboard technique for placing
a patient on a long backboard (a spinal immobilization device upon
which patients sus-pected of having spinal column traumas are placed).
Log rolling requires the help of several people

[CT
scanning allows a detailed view of intra-abdominal pathology. However,
most scanners are located a distance from the emergency department and
the patient must be stable before transfer. Use of a double contrast technique
also necessitates a delay before scanning can commence of typically 40
minutes to 1 hour]

anamnesis & allergies, medications, past medical
history (PMH)/past surgical history (PSH), last meal, events
or environment related to injury (AMPLE) to provide a more ample history
with which to work

a SNP in caspase-12,
confined to individuals of African descent, results in the production of
a full-length caspase-12 precursor protein (Csp12-L), instead of a truncated
caspase-12 protein (Csp12-S), leading to reduction in LPS-induced cytokine
production and subsequently an enhanced susceptibility to bacterial invasion
of the bloodstream (septicaemia) and increased mortality. Csp12-L might
function as a dominant negative regulator of the activity of other caspases,
potentially by antagonizing the inflammasome (the protein scaffold within
which active cytokines are produced) and the associated pro-inflammatory
pathways. Csp12-S was also found to inhibit NF-kB
activation, although to a lesser extent than Csp12-L. Caspase-12 antagonists
might have therapeutic potential for treating septic shockref

amniotic infection syndrome of Blane : a syndrome in which fetal
sepsis follows swallowing and at times aspiration of contaminated amniotic
fluid.

neonatal sepsis

early onset neonatal
sepsis (EONNS) : illness appearing from birth to 7 days (90% within
24 hours, 8% between 24 and 48 hours after delivery, and 2% between 48
hours and 6 days after delivery). If affects term newborns; onset is more
rapid in preterm newborns (often infection caused preterm delivery). The
infection (pneumonia or systemic) was acquired by mother and transmitted
to the fetus via :

group B Streptococcus
spp.
: the recommendation for universal prenatal screening of pregnant women
late in pregnancy was maderef.
It would seem that the absence of universal screening might increase the
number of cases but not the case fatality rate. This is a summary of the
pertinent recommendations:

recommendation of universal prenatal culture-based screening for vaginal
and rectal GBS colonization of all pregnant women at 35-37 weeks' gestation.

recommendation against routine intrapartum antibiotic prophylaxis for GBS-colonized
women undergoing planned cesarean deliveries who have not begun labor or
had rupture of membranes.

penicillin remains the 1st line agent for intrapartum antibiotic prophylaxis,
with ampicillin an acceptable alternative. For penicillin-allergic women
at high risk for anaphylaxis, testing of GBS isolates from prenatal screening
for susceptibility to clindamycin and erythromycin is recommended, if feasible.
One of these agents should be employed for intrapartum GBS prophylaxis
if the screening isolate is susceptible to both agents. Vancomycin should
be reserved for penicillin-allergic women at high risk for beta-lactam
anaphylaxis when clindamycin or erythromycin are not options because of
in vitro resistance or unknown susceptibility of a prenatal isolate.

women whose culture results are unknown at the time of delivery should
be managed according to the risk-based approach; the obstetric risk factors
remain unchanged (i.e., delivery at <37 weeks' gestation, duration of
membrane rupture >18 hours, or temperature >100.4°F [>38.0°C]).

Buhl's disease : an acute sepsis affecting newborn infants, marked
by hemorrhages into the skin, mucous membranes, and navel attended with
cyanosis and jaundice; there are also hemorrhages in the intestinal organs.

Laboratory examinations : in the first 48
hours after delivery, many laboratory values may experience wide excursions
due to stress of labor, adaptation to extrauterine life, and placental
expulsion or secretion

culture of blood and other sterile fluids (urine, CSF) or surface,
smear and Gram staining, antigen research test. Blood culture (the gold
standard) has poor sensitivity as antibacterials have been administered
to the mother during labor, bacteremia is intermittent or transient, a
poor blood quantity has been sampled, suboptimal blood processing and results
only after 1-3 days (95% are positive after 48 hoursref).
Only 12% of newborns at risk for sepsis have positive blood cultureref.
Only 1 septic newborns occurs every 17-30 broad-spectrum antibacterial-treated
newborns, lading to emergence of opportunistic bacteria, antibacterial
resistance, and high healthcare expenditures.

[CRP]plasma > 10 mg/L. Synthetized by hepatocytes induced by
IL-1b, IL-6 or TNF; rise after 5-6 hours, peak
after 36-50 hours, not affected by gestational age; increased in PROM,
maternal fever, chorioamnionitis,
asphyxia, cerebral hemorrhage,
IRDS,
and MAS,
but also in 8% of healthy newborns. Limited value in the first 12-24 hours;
variable response to non-bacterial infections; useful in follow-up of antibiotic
therapy

Anyway some patients without apparent clinical symptoms of sepsis nevertheless
present high serum CTpr levels, and some patients with a syndrome meeting
the commonly accepted criteria for sepsis do not have high levels. Moreover,
the clinical diagnosis of sepsis is often subjective and hence not infrequently
uncertain. For example, a patient with SIRS and positive blood cultures
clearly merits a clinical diagnosis of sepsis, while a patient with SIRS,
consistently negative blood cultures and a localised bacterial infection
(e.g. pneumonitis or pyelonephritis), may or may not be considered septic.
Thus, evaluation of the reliability of a marker for sepsis is contingent
upon the accuracy of the clinical diagnosis. A serum CTpr level must be
evaluated with proper consideration of the clinical and laboratory context.
Finally, whether or not SIRS is present, there is an overlap of serum CTpr
values between patients with marked systemic inflammation and those with
either a presumptive or definitive clinical diagnosis of sepsis.

microarray
expression profiles can be used to diagnose sepsis, distinguishing in vivo
between sterile and infectious causes of systemic inflammation.Exploratory
studies were conducted using spleens from septic patients and from mice
with abdominal sepsis. Seven patients with sepsis after injury were identified
retrospectively and compared with 6 injured patients. C57BL/6 male mice
were subjected to cecal ligation and puncture, or to IP lipopolysaccharide.
Control mice had sham laparotomy or injection of IP saline, respectively.
A sepsis classification model was created and tested on blood samples from
septic mice. Accuracy of sepsis prediction was obtained using cross-validation
of gene expression data from 12 human spleen samples and from 16 mouse
spleen samples. For blood studies, classifiers were constructed using data
from a training data set of 26 microarrays. The error rate of the classifiers
was estimated on seven de-identified microarrays, and then on a subsequent
cross-validation for all 33 blood microarrays. Estimates of classification
accuracy of sepsis in human spleen were 67.1%; in mouse spleen, 96%; and
in mouse blood, 94.4% (all estimates were based on nested cross-validation).
Lists of genes with substantial changes in expression between study and
control groups were used to identify 9 mouse common inflammatory response
genes, six of which were mapped into a single pathway using contemporary
pathway analysis toolsref

MATISSE is a new endotoxin (ET) adsorption system comprising the
FRESENIUS hemoadsorption machine 4008 ADS to maintain the extracorporeal
circuits and disposables including the MATISSE-adsorber based on macroporous
beads immobilized with human serum albuminref

direct hemoperfusion (DHP) with an adsorbent column using polymyxin
B-immobilized fiber (PMX-F) has been shown to improve the state of
shock in patients with septic shock. However, no evidence has been presented
for a direct link between endotoxin removal by DHP with PMX-F and improvement
in septic shock. We retrospectively analyzed clinical profiles of 24 patients
with septic shock (16 patients, gram-negative; 8 patients, non-gram-negative
septic shock) who underwent DHP with PMX-F. Patients with gram-negative
septic shock were characterized by hyperdynamic circulation. DHP with PMX-F
reduced blood endotoxin concentrations and ameliorated shock, with an improvement
in hyperdynamic circulation in patients with gram-negative septic shock.
Mean arterial pressure also was elevated after therapy in patients with
non-gram-negative septic shock, but systemic hemodynamics were unaffected.
Regardless of the causative microorganism, patients with endotoxemia (blood
endotoxin level > 10 pg/mL) showed hyperdynamic shock, and DHP with PMX-F
reduced blood endotoxin levels and ameliorated hyperdynamic circulation,
whereas patients without endotoxemia showed features of shock without hyperdynamic
circulation, and DHP with PMX-F ameliorated shock without affecting cardiac
performance. In patients with gram-negative septic shock, blood endotoxin
concentration correlated positively with cardiac output and negatively
with systemic vascular resistance before DHP therapy. Reduction in blood
endotoxin concentration by DHP therapy positively correlated with the reduction
in cardiac output. The improvement in hyperdynamic circulation was related
directly to endotoxin removal by the PMX-F column, and endotoxin has an
important role in the development of hyperdynamic circulation in patients
with gram-negative septic shockref1,
ref2,
ref3

The endotoxin adsorber system did not result in a significantly improved
primary end point in patients with presumed Gram-negative sepsis. In patients
with peritonitis, the adsorber treatment likewise did not result in significantly
improved APACHE II scoresref

those that have worked in rodents but not in humans :

96-hour infusion (24 mg/kg of body weight per
hour)) of recombinant human activated
protein C (APC)
administered within 24 hours of onset helps to thin blood, break up clots
and reduce inflammation, which lowers the number of sepsis-related deaths
by around 7%ref1,
ref2.
Anyway the ADDRESS (Administration of Drotrecogin Alfa [Activated] in Early
Stage Severe Sepsis) trial showed no benefit of drotrecogin alfa (activated)
(DrotAA) in patients with severe sepsis and a low risk of death (defined
by single-organ failure or an APACHE II score
<25)ref

cell-penetrating lipopeptides—termed pepducins—that target either
individual or multiple chemokine receptors. IL-8,
a ligand for the CXCR1
and CXCR2
receptors, is the most potent endogenous proinflammatory chemokine in sepsis.
IL-8 levels rise in blood and lung fluids to activate neutrophils and other
cells, and correlate with shock, lung injury and high mortality. Pepducins
derived from either the i1 or i3 intracellular loops of CXCR1 and CXCR2
prevent the IL-8 response of both receptors and reverse the lethal sequelae
of sepsis, including disseminated intravascular coagulation and multi-organ
failure in mice. Conversely, pepducins selective for CXCR4 cause a massive
leukocytosis that does not affect survival. CXCR1 and CXCR2 pepducins conferred
nearly 100% survival even when treatment was postponed, suggesting that
this approach might be beneficial in the setting of advanced diseaseref.

intravenous infusion of >97% purified vitamin
B2 / riboflavin 5'-sodium phosphate
at doses of 2.5, 5, 10, and 20 mg/kg of body weight (doses above those
used clinically to treat vitamin B2 deficiency), 14-days survival
levels were 35%, 65%, 90%, and 95%, respectively. Moreover, treatment with
vitamin B2 at 20 mg/kg 6 h after LPS injection not only lowered
levels of excessive plasma proinflammatory cytokines, including TNF-a,
IL-1b, IL-6, IFN-g,
MCP-1, and MIP-2, but also decreased NO levels. Vitamin B2 is
best known for its ability to help the body process proteins, fats and
carbohydrates but it can also enhance host resistance to infectionref,
stimulated neutrophil functionsref,
and boosted macrophage function (Kimura, M., M. Suzuki, and S. Araki. 1996.
In vitro and in vivo effects of riboflavin sodium phosphate on the phagocytic
activity of peritoneal macrophages in mice. Anim. Sci. Technol. 67:368-373).
It bursts 1-week survival in rodents inoculated with sepsis-causing Escherichia
coli
from 10% to 95% by speeding the clearance of bacteria from the body and
lowering levels of molecules that cause inflammationref

cryptogenic septicemia : septicemia
in which the focus of infection is not evident during life.

metastasizing
or phlebitic septicemia / pyemia / metastatic infection : a general
septicemia in which secondary foci of suppuration occur and multiple abscesses
are formed. The condition is marked by fever, chills, sweating, jaundice,
and abscesses in various parts of the body

arterial pyemia : a form due to the
dissemination of septic emboli from the heart.

cryptogenic pyemia : that in which the source of infection is unidentified.

puerperal fever, sepsis orsepticemia
/ childbed fever : septicemia accompanied by fever, in which the focus
of infection is the uterus; the etiologic agent is frequently a streptococcus

sputum septicemia : a form produced
by inoculation of certain of the microorganisms of the sputum.

fish-slime disease : septicemia
following a puncture wound made by the spine of a fish.

Pathogenesis : there is a correlation between
excessive production of C5a
during the onset of sepsis and poor clinical outcome associated with compromised
innate immunity as CD88 / C5aR
triggering reduces degradation of IkB. An increased
level of IkB results in decreased NF-kB
activity and, therefore, decreased TNF-a
transcription by neutrophils, one of the innate defences in response to
bacteria
Symptoms & signs : as above + mental
impairment
Laboratory examinations : as above +

septic shock : shock associated with
overwhelming infection. It is thought to result from the action of endotoxins
by gram-negative bacteria
(endotoxic or endotoxin
shock) or other products of the infectious agent on the vascular system
causing large volumes of blood to be sequestered in the capillaries and
veins; activation of the complement
system
and kinin system and the release of histamine, cytokines (toxic
shock : associated with release of TNF-a
by host mononuclear cells), prostaglandins, and other mediators may be
involved

intensive insulin
therapy to achieve a strict normalization of blood glucose levels significantly
reduced morbidity but not mortality among all patients in the medical ICU.
Although the risk of subsequent death and disease was reduced in patients
treated for three or more days, these patients could not be identified
before therapyref

Experimental animal models :

intravenous infusion of LPS
into mice or rats : this causes an early (< 4 hours) high level
of TNF in the plasma followed by shock and death. Prior administration
of LPS-specific or TNF-a-specific
antibody is protective and greatly improves survivalref1,
ref2.
In humans with sepsis, LPS-specific or TNF-specific antibody has not been
protective in clinical trials. This might be due to the fact that LPS models
in rodents do not reflect conditions found in humans with sepsis. LPS has
been infrequently found in the plasma of humans with sepsis. Plasma levels
of TNF are low and transient in humans compared with levels found in miceref.
For all of these reasons, the LPS model in rodents might not be relevant
to human sepsis.

intravenous infusion of live bacteria into various laboratory animals
: infusion or large amounts of live bacteria (Escherichia
coli
or Pseudomonas spp.)
results in cardiovascular collapse, shock, diffuse activation and consumption
of the clotting and fibrinolytic systems, and death. In humans with sepsis,
the presence of bacteria in the blood sometimes occurs. When detectable
in human blood, the number of bacteria is markedly lower than the amounts
of infused intravenously into animals. The animal models of overwhelming
bacteraemia have questionable relevanc to humans with sepsis, even though
the animals show evidence of MOF in which lung, liver and renal functions
deteriorate, similar to humans with fatal sepsis.

caecal ligation
and puncture (CLP) in rats and mice : this model results in peritonitis
and bacteremia (with presence of Gram-negative aerobic and anaerobic bacteria
- polymicrobial sepsis - from the gut flora). Depending on the number and
size of caecal punctures, the model can allow survival or can be lethal.
In many respects, this model mimics the clinical course of sepsis in humans,
with an early hyperdynamic phase (increased HR and CO, increased BR, fever
and leukocytosis). This is followed by a hypodynamic phase, with reduced
CO and HR, reduced BR, decreasing body temperature (hypothermia) and the
onset of shock and lethality. This model has only been used in rodents.
The CLP model seems to be a reasonable surrogate for sepsis in humans.

severity of disease indices (SDI) are used to define death RR, standardize
and support therapies and compare ICUs. The greater the number of variables
evaluated, the lesser the error. SDIs are obtained by :

death : the cessation of life; permanent cessation
of all vital bodily functions. For legal and medical purposes, the following
definition of death has been proposed—the irreversible cessation of all
of the following: (1) total cerebral function, (2) spontaneous function
of the respiratory system, and (3) spontaneous function of the circulatory
system. It is a state in declining evolution, included between cessation
of activity of nervous centres, brain, and breath, and extinction of last
cell groups. The sensitivity of tissues to systemic
acute hypoxia
is as follows : encephalon (cortex > encephalic nuclei > brainstem) > liver
> kidneys > heart > lungs > cornea > skin > skin adnexa > spermatozoa (days)
> blood (6 hours : sampling was practiced in ex-USSR, but not in Italy)

Grading :

local death : death of a part of the body.

systemic death

relative death : recovery still possible

intermediate death : any likelihood of recovery can be excluded

absolute, real, somatic or biological death : definitive biological
silence (extinction of the last cell groups)

Laboratory examinations : death was once assessed
looking for opacization of glasses placed at body orifices, then by listening
at carotid and radial pulses, and finally with wood stethoscope.

preagonal : preceding the death agony

premortal : occurring just before death

moribund : in a dying state

agony : old term for the period just before
death occurs, which was thought to be a time of extreme pain.

apparent death (suspended animation):
a state of complete interruption of bodily processes from which the patient
can be resuscitated. As it is appreciated only with electrodiagnosis, always
continue cardiopulmonary
resuscitation (CPR)
maneuvers for 30'.

functional death : total, permanent destruction of cognition and
related higher functions of the CNS, with vital functions being sustained
by artificial means.

decerebrate : a person with brain damage resulting in neurologic
signs similar to those of a decerebrated animal; the human brain lesion
may differ somewhat from that of an experimental animal; bulbar depression
may require even 30 minutes of anoxia, according to temperature

decorticate :

cardiac death : assessed with EKG for 20 minutes

respiratory death : assessed with ABG

Age of death :

fetal death / stillbirth : death in utero; failure of the
product of conception to show evidence of respiration, heart beat, or definite
movement of a voluntary muscle after expulsion from the uterus, with no
possibility of resuscitation

early fetal death : fetal death occurring during the first 20 weeks
of gestation.

intermediate fetal death : fetal death occurring during the 21th
to 28th weeks of gestation.

late fetal death : fetal death occurring after 28 weeks of gestation.

Aetiology : leading cause of death
10 leading causes of death in all WHO member states, 2000 :

cause

% of total

(1) ischemic heart disease

12.4%

(2) cerebrovascular disease

9.2%

(3) lower respiratory infections

6.9%

(4) HIV/AIDS

5.3%

(5) chronic obstructive pulmonary disease

4.5%

(6) perinatal conditions

4.4%

(7) diarrhoeal diseases

3.8%

(8) tuberculosis

3.0%

(9) road traffic injuries

2.3%

(10) trachea, bronchus, lung cancers

2.2%

USA, 2002

formal name

informal name

% of all deaths

(1) diseases of the heart

heart attack (mainly)

28.5%

(2) malignant neoplasms

cancer :

lung : 30.9% (154,900)

colon : 9.6% (48,100)

breast : 8.0% (40,000)

prostate : 6.0 (30,200)

pancreas : 5.9% (29,700)

lymphoma : 5.2% (25,800)

leukemia : 4.3% (21,700)

22.8%

(3) cerebrovascular disease

stroke

6.7%

(4) chronic lower respiratory disease

emphysema, chronic bronchitis

5.1%

(5) unintentional injuries

accidents :

motor vehicle accidents (MVA) : 44.3%

between vehicles : 43%

with fixed object : 27%

pedestrian : 16% (65% were urban)

noncollision : 10%

collision pedacycle : 2%

collision train : 1%

50% were at night

50% involved intoxicants in driver

62% were rural

25% of urban MVA deaths were pedestrian

55% involved traffic violations

driving at unsafe speed : 16.5%

failure to yield right-of-way : 7.8%

crossed the centre line : 7.5%

passed stop sign : 2.6%

improper overtaking : 2.5%

disregarded a signal : 2.2%

followed too closely : 0.6%

other violations : 15.3%

falls : 17.8%

poison : 13-0%

drowning : 3.9%

fires, burns, smoke : 3.4%

medical/surgical complication : 3.1%

other land transport : 1.5%

firearms : 0.8%

others (nontransport) : 17.8%

44% of non-motor vehicle accidents occurred in the home: in 1992

falls 31.8%

poison(sol/liq) 21.0%

fire,burns 16.4%

obstructed airway 8.7%

suffocation 3.6%

firearms 2.6%

poison(gas) 2.1%

all other 13.8%

4.4%

(6) diabetes mellitus

diabetes

3.0%

(7) influenza and pneumonia

flu & pneumonia

2.7%

(8) Alzheimer's disease

Alzheimer's senility

2.4%

(9) nephritis and nephrosis

kidney disease

1.7%

(10) septicemia

systemic infection

1.4%

(11) intentional self-harm

suicide

1.3%

(12) chronic liver/cirrhosis

liver disease

1.1%

(13) essential hypertension

high blood pressure

0.8%

(14) assault

homicide

0.7%

(15) all other causes

other

17.4%

USA, 1998 : 5 leading causes of death ages 15-24 years :

5 leading % of top LEADING PERCENT OF TOP 5CAUSES OF DEATH, USA, AGES 15-24,
1998

sudden infant death
syndrome (SIDS) : the sudden and unexpected death of an apparently
healthy infant (50-63% of these infants have a preexisting URT infection
before death), typically occurring between the ages of 3 weeks and 6 months,
and not explained by careful postmortem studies (diagnosis of exclusion).
In 1956, Barrattref introduced the term "cot death" (crib death)
to describe unexpected infant deaths without obvious explanation. The term
highlights the common feature that many of these infants are discovered
dead in their cots. The term sudden unexpected death in infancy (SUDI)
provides
a broader designation, which includes cot deaths. After thorough post-mortem
enquiries, sudden unexpected deaths in infancy divide into various explained
deaths and a residual group for which no explanation can be found, designated
sudden infant death syndrome (SIDS). It has long been recognised that some
sudden unexpected deaths in infancy are not naturalref1,
ref2,
ref3.
Starting from the assumptions that "SIDS deaths appear to occur in families
at random" and that "there is no evidence of a genetic etiology", DiMaio
and DiMaio concluded that "Siblings of SIDS have the same risk as the general
population". They therefore implicitly derived the probability of two or
three SIDS deaths occurring in one family by squaring or cubing the probability
of a single death. This approach led them to conclude that "while a second
SIDS with one mother is improbable, it is possible . . . " or " . . . remotely
possible . . . " (2nd edition) and "A third case, in our opinion is not
possible and is a case of homicide". Meadowref
and the Confidential Enquiry into Stillbirths and Deaths in Infancy (CESDI)
in their report on Sudden Unexpected Death in Infancy (SUDI) used a similar
argument for deducing the probability of two SIDS deaths. Meadow, apparently
following the DiMaios' lead, wrote in the third edition of the ABC of Child
Abuse that "2 is suspicious and 3 murder unless proved otherwise . . .
is a sensible working rule for anyone encountering these tragedies". The
assumptions of independence that underlie these estimates are invalid,
because siblings have 25% of genes in common and experience an essentially
similar domestic environment, which might, however, be altered by the preceding
death. Several studies have shown that siblings of infants with SIDS are
at increased risk of SIDSref.
The best estimate was given by the Norwegian population-based study, which
reported that the relative risk of recurrence was 5·8 (95% CI 2·1-13·2).
Such studies of recurrence have been criticised for not considering the
possibility of serial infanticide. However, a review of the accuracy of
the diagnosis of SIDS in Norway during the period of the study suggested
that SIDS was originally substantially underdiagnosed. Nevertheless, the
risk of recurrence is sufficiently low to exclude the possibility of a
simple inheritance pattern for SIDS. In consideration of whether repeated
unexpected infant deaths in a family are natural or not, isolated estimates
of the probability of > 1 SIDS case in a family, however derived, are invalid
and easily misinterpreted. Multiple infanticide is also very rare. What
is important is the relative likelihood that the deaths are natural versus
unnatural, given that 2 or more deaths have occurred. Such information
can be obtained only from unselected series of families who have had more
than one unexpected infant death. Emery, who was concerned about filicide
and also undetected hereditary disease, in a personal series of casesref
reported that filicide was probable in 5 of 12 cases of 2 or more unexpected
deaths in a family. He and colleagues reported similar results in another
10 unselected cases of repeated unexpected infant deathsref.
Stantonref,
in a follow-up study of unselected cases, has recently reported 3 families
who each had had 2 unexpected infant deaths, 2 of which raised maltreatment
issues. Second deaths are not rare and that the majority, 80-90%, are natural.
Families who have experienced three unexpected deaths also occur. The study
included 2 families in which there were 2 CONI deaths--one triple SIDS
and one triple filicideref.

Epidemiology : incidence of SIDS = 1-3%
(the most common cause of death for babies between 1 month and 1 year old
in the developed world). 3,000 US infants a year, significantly higher
in African-Americans.
Aetiology :

sudden
infant death and dysgenesis of the testes syndrome (SIDDT) (autosomal
recessive, common in Pennsylvania's Amish and Mennonite communities that
have lost 21 babies in 2 generations) : such babies die before they are
1 year old from sudden cardiac and respiratory failure. Males with the
syndrome may have underdeveloped testes, but girls appear normal, with
normal female hormones

polymorphisms in the serotonin
transporter
gene promoter region and in intron 2 are more common among SIDS cases compared
with control subjects. Genes pertinent to early embryologic development
of the autonomic nervous system (ANS), including MASH1, BMP2,
PHOX2a, PHOX2b, RET, ECE1, EDN1, TLX3, and EN1 : 11 protein-changing rare
mutations have been identified in 14 of 92 SIDS cases among the PHOX2a,
RET, ECE1, TLX3, and EN1 genes, while only 1 of these mutations (TLX3)
has been identified in 2 of 92 control subjects. Black infants accounted
for 10 of these mutations in SIDS cases and 2 control subjects. 4 protein-changing
common polymorphisms were identified in BMP2, RET, ECE1, and EDN1, but
the allele frequency did not differ between SIDS cases and control subjects.
However, among SIDS cases, the allele frequency for the BMP2 common polymorphism
demonstrated ethnic differences; among control subjects, the allele frequency
for the BMP2 and the ECE1 common polymorphisms also demonstrated ethnic
differences : 71% of the SIDS cases that had the mutation were African-American
and both controls (healthy babies that had it) were African-Americanref

mutations in the mitochondrial genes MTTL1
and MTND1
may play a role in some cases of SIDS

mutations in the cardiac sodium channel gene SCN5A
and the KCNQ1
gene that cause long QT syndrome

protracted intrauterine hypoxia or recurrent hypoxic insults during
fetal life undoubtedly influence the development of the central nervous
structures as a tissue most susceptible to hypoxia, although well developed
mechanisms of defense against hypoxia exist during the fetal life. The
mechanisms underlying SIDS include neurologically compromised infants who
are deprived of compensatory mechanisms during sleep, sustaining a hypoxic
insult with alterations in neurotransmitter receptors within the regions
involved in chemoreception and cardiovascular control. Changes in the brain
result from perinatal prolonged hypoxia (persistent reticular pathways
in the pons and medulla, astroglia in the brainstem, gliosis of brain nerve
nuclei, defects in neurotransmitter receptors, neuronal apoptosis, microthrombosis,
and hypoxic ischemic lesion). Hypoxic perinatal risk factors for SIDS included

passive and active exposure to cigarette
smoking
in pregnancy : as cigarette smoking has been demonstrated to lead to fetoplacental
insufficiency, which result in fetal hypoxia, it is concluded that hypoxia
is a precondition for the occurrence of SIDS. Prenatal exposure to cigarette
smoke decreases maternal RBC count, and concentrations of tyrosine and
selenium, reduces fetal and neonatal CBF, and increases maternal MCV, leukocytosis,
especially neutrophils, monocytes and lymphocytes, maternal and fetal heart
rate, systolic and diastolic blood pressure, resistance index in umbilical
artery, fetal hemoglobin, cytokine, serotonine, dopamine, catecholamine,
hypoxanthine, endorphin and IL-6. Maternal smoking and illness =>
uncontrolled inflammatory response to infection predominantly occurring
at night-time. The immature immune system may be altered by a primary infection,
preventing a protective response after secondary challenge

increased levels of HVR-I substitutions may be an indicator of mtDNA
instabilityref

mors thymica : a type of SIDS or death
of a child formerly thought to occur in thymic asthma and status lymphaticus
/ status thymicolymphaticus / status thymicus (developmentally normal
hyperplasia of lymphoid tissue and the thymus, formerly thought to be an
important cause of SIDS by airway obstruction)

Prevention : to best protect babies from sudden
infant death syndrome, or SIDS, they should be offered pacifiers and should
not sleep on their sides because infants often roll over onto their stomachs.
It's not clear why pacifiers protect against SIDS : maybe it's more difficult
to roll onto their faces with a pacifier, or they could be lighter sleepers
if they're using pacifiers. Pacifiers shouldn't be coated with any sweet
liquid or reinserted during sleep, and babies shouldn't be forced to take
them. Infants also are least likely to get SIDS if they sleep on hard mattresses
without pillows, comforters or other soft objects. Babies should sleep
near parents, but in their own beds. Although the percentage of babies
sleeping prone plummeted from 1992 to 2002, more black infants (82% in
1992, 19% in 2002) than whites (71% in 1992, 12% in 2002) are still put
to sleep on their tummies; the SIDS rate for blacks is 2.5 times higher
(2.2 per 1,000 live balck births in 1992; 1.2 in 2002)) than for whites
(1.0 in 1992, 0.5 in 2002). Babies in child care also are at higher-than-average
risk. About 17% of SIDS cases occur at day care, but < 10% should happen
there, based on Census figures. The SIDS rate is highest in family day-care
homes, Moon's research shows. It's unknown why, as babies are no more likely
to sleep prone in day care than at homeref

sudden unexplained
death syndrome (SUDS) : death for which no underlying cause can be
found of a person 2 years old or older, observed particularly in those
of Southeast Asian origin